Abstract

ABSTRACT Lead levels in whole blood and in plasma were measured in 64 non-exposed and in 29 exposed subjects with signs and symptoms of varying severity. Lead was determined by atomic absorption spectrophotometry after chelation with ammonium pyrrolidine dithiocarbamate and extraction with methyl isobutyl ketone. The method has a sensitivity of 0·4 μg/100 ml (0·02 μmol/l) for whole blood and of 0·2 μg/100 ml (0·01 μmol/l) for plasma and is reliably accurate and precise. Plasma lead increases progressively and significantly with the increase of whole blood lead, while its relative percentage in the plasma remains practically constant at all concentrations in whole blood. In exposed subjects a highly significant correlation was found between lead in plasma and lead in urine (r = 0·549) but the correlation coefficient was higher for whole blood lead versus urinary lead (r = 0·938). Aminolevulinic acid excretion in urine appeared to be significantly related to plasma lead concentration (r = 0·563) but to a greater extent to whole blood levels (r = 0·801). There was no significant correlation between lead in plasma and the logarithm of aminolevulinic acid dehydratase. The hypothesis is advanced that plasma lead, the more biologically active fraction of the metal, could be related to different individual sensitivities which would condition the development of toxic effects in various organs at different levels of lead.